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Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons
Journal article   Peer reviewed

Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons

D L Pettit, S Perlman and R Malinow
Science (New York, N.Y.), Vol.266(5192), pp.1881-1885
12/16/1994
DOI: 10.1126/science.7997883
PMID: 7997883

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Abstract

Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.
Recombinant Proteins - metabolism Cell Line Synaptic Transmission - physiology 2-Amino-5-phosphonovalerate - pharmacology Rats Pyramidal Cells - enzymology Hippocampus - cytology Vaccinia virus - genetics Patch-Clamp Techniques Animals Transfection Long-Term Potentiation - drug effects Membrane Potentials Pyramidal Cells - physiology Long-Term Potentiation - physiology Hippocampus - enzymology Synaptic Transmission - drug effects Genetic Vectors Hippocampus - physiology In Vitro Techniques Calcium-Calmodulin-Dependent Protein Kinase Type 2 Calcium-Calmodulin-Dependent Protein Kinases - metabolism Vaccinia virus - physiology

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